MOM-5 frizzled regulates the distribution of DSH-2 to control C. elegans asymmetric neuroblast divisions
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Updated: Aug 17, 2026

Live-cell Imaging of Sensory Organ Precursor Cells in Intact Drosophila Pupae
Published on: May 27, 2011
Nancy C Hawkins1, Gregory C Ellis, Bruce Bowerman
1Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA. nhawkins@sfu.ca
Abstract:
Asymmetric cell divisions produce all 302 neurons of the C. elegans hermaphrodite. Here, we describe a role for a C. elegans Dishevelled homolog, DSH-2, in an asymmetric neuroblast division. In dsh-2 mutants, neurons normally descended from the anterior neuroblast daughter of the ABpl/rpppa blast cell were frequently duplicated, while non-neuronal cells produced by the posterior daughter cell were often missing. These observations indicate that in the absence of dsh-2 function, the posterior daughter cell was transformed into a second anterior-like cell. Loss of mom-5, a C. elegans frizzled homolog, produced a similar phenotype. We also show that the DSH-2 protein localized to the cell cortex in most cells of the embryo. In the absence of MOM-5/Fz, DSH-2 was localized to the cytoplasm, suggesting that MOM-5 regulates asymmetric cell division by controlling the localization of DSH-2. Although all neurons in C. elegans are produced by an invariant pattern of cell divisions, our results indicate that cell signaling may contribute to asymmetric neuroblast division during embryogenesis.
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